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Delta and Egfr expression are regulated by Importin-7/Moleskin in Drosophila wing development

机译:Delta和Egfr表达受果蝇翅膀发育中Importin-7 / Moleskin的调控

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摘要

Drosophila DIM-7 (encoded by the moleskin gene, msk) is the orthologue of vertebrate Importin-7. Both Importin-7 and Msk/DIM-7 function as nuclear import cofactors, and have been implicated in the control of multiple signal transduction pathways, including the direct nuclear import of the activated (phosphorylated) form of MAP kinase. We performed two genetic deficiency screens to identify deficiencies that similarly modified Msk overexpression phenotypes in both eyes and wings. We identified I I total deficiencies, one of which removes the Delta locus. In this report, we show that Delta loss-of-function alleles dominantly suppress Msk gain-of-function phenotypes in the developing wing. We find that Msk overexpression increases both Delta protein expression and Delta transcription, though Msk expression alone is not sufficient to activate Delta protein function. We also find that Msk overexpression increases Egfi- protein levels, and that msk gene function is required for proper Egfr expression in both developing wings and eyes. These results indicate a novel function for Msk in Egfr expression. We discuss the implications of these data with respect to the integration of Egfr and Delta/Notch signaling, specifically through the control of MAP kinase subeellular localization. (c) 2007 Elsevier Inc. All rights reserved.
机译:果蝇DIM-7(由痣皮基因msk编码)是脊椎动物Importin-7的直系同源物。 Importin-7和Msk / DIM-7均起核输入辅助因子的作用,并已参与多种信号转导途径的控制,包括MAP激酶活化(磷酸化)形式的直接核输入。我们进行了两个遗传缺陷筛查,以鉴定在眼睛和翅膀上都相似地修饰了Msk过表达表型的缺陷。我们确定了我的全部不足之处,其中之一消除了Delta基因座。在这份报告中,我们显示了功能丧失的Delta等位基因主要抑制了发育中翼的Msk功能获得的表型。我们发现Msk过表达增加了Delta蛋白表达和Delta转录,尽管仅Msk表达不足以激活Delta蛋白功能。我们还发现,Msk过表达会增加Egfi蛋白水平,并且在发育中的翅膀和眼睛中正确的Egfr表达都需要msk基因功能。这些结果表明Msk在Egfr表达中的新功能。我们讨论有关Egfr和Delta / Notch信号整合的这些数据的含义,特别是通过控制MAP激酶的细胞外定位。 (c)2007 Elsevier Inc.保留所有权利。

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